The mechanisms by which inflammation affects tight junction structure and function and transcellular mechanisms such as endocytosis are largely unknown, although reproducible correlations have been observed between the severity of experimental and clinical disease and on the one hand and transepithelial electrical resistance, transport of paracellular markers, and systemic LPS concentrations and on the other [42, 86]
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Resistant cells generate more glutathione, elicit nuclear factor erythroid 2-related factor 2 (NRF2) activation, and overexpress many anti-oxidative genes such as superoxide dismutase, catalase, glutathione peroxidase, and thioredoxin reductase, providing stronger antioxidant capacity to survive in a more oxidative environment due to the sharp rise in oxidative metabolism and reactive oxygen species generation
These cellular security guards express TLRs used to sense and endocytose bacterial products and also promote the downstream activation and release of inflammatory mediators (Birchenough et al
